1. Field of the Invention
The present invention generally relates to catheters used during surgery and, more particularly, to an umbrella style catheter which is temporarily placed in the main pulmonary trunk of a patient to detect, prevent and treat pulmonary emboli.
2. Description of the Prior Art
Pulmonary embolism is one of the most misdiagnosed of the serious acute disorders encountered by clinicians and is estimated to be the third most common cause of death in the United States. As many as 200,000 people die each year as a result of pulmonary embolism. Approximately 650,000 patients in the United States are affected by symptomatic pulmonary embolism each year. As many as sixty percent of the patients who develop pulmonary embolism are not diagnosed as having the condition until after their death. If no specific treatment is initiated following pulmonary embolism, the incidence of fatal recurrent embolism is approximately thirty percent.
Thrombi or blood clots can form in a patient's veins, particularly large veins, under certain conditions and these blood clots can dislodge from the veins and travel to the lungs where they can occlude the pulmonary vessels. The impact that thrombi which have dislodged and travelled to a patient's lungs can have on the patient can vary from sudden death to no perceptible change in well being. The following have been described as the primary sites of thrombus formation: (1) the iliac vein (especially the external iliac vein), (2) the common femoral or proximal thigh vein, (3) the termination of the deep femoral vein, (4) the popliteal vein, (5) the posterior tibial vein, and (6) the calf veins. Thrombi in the calf veins are the most common, but are the least likely to embolize. Thrombi in the proximal thigh and iliac veins are most likely to embolize.
The formation of a clot in the veins involves either injury to the vessel wall and/or associated slowing of blood flow. The production of a permanent hemostatic plug results from the combined activities of endothelial cells, platelets, red cell, and coagulation cascade. When venous thrombi dislodge from their site of formation, they flow with the blood through the venous system to the pulmonary circulation. If the thrombus is extremely large, it can stop at the bifurcation of the pulmonary artery and form a "saddle embolus" which is instantly fatal. The majority of emboli dislodge to distal parts of the lung.
Emboli in lobar and segmental pulmonary arteries are associated with humoral vasoconstriction and bronchoconstriction which are known to potentiate vascular injury in patients without prior cardiopulmonary disease. Right ventricular afterload increases when the pulmonary artery obstruction reduces the vascular bed by greater than twenty five percent. To compensate for such an impairment, the right ventricular and pulmonary artery pressures rise. A normal right ventricle can generate a maximum pulmonary artery systolic pressure of approximately 40 mm Hg at standard temperature and pressure. As the right ventricular outflow pressure rises acutely, the right ventricle dilates and becomes hypokinetic and fails, resulting in cardiogenic shock. When cardiac function has been compromised by previous cardiopulmonary illness, relatively smaller emboli obstructing only one or two segments can exert a similar hemodynamic effect. Because of the anatomical juxtaposition of the two ventricles, right ventricular dilation adversely affects the left ventricular filling function and can cause left ventricle failure as well.
Pulmonary embolisms have been classified into three broad categories: Massive Pulmonary Embolism, Submassive Pulmonary Embolism, and Smaller Pulmonary Embolism. Massive pulmonary embolism results from a twenty five percent or greater obstruction of the pulmonary vascular bed. The most common symptoms of massive pulmonary embolism are fainting, corpulmonale, and cardiogenic shock or cardiac arrest. Submassive pulmonary embolism can be defined as an embolism to one or more pulmonary segments not accompanied by elevation in right ventricular and pulmonary artery systolic pressures. The most frequent symptoms of submassive pulmonary embolism are dyspnea and pleuritic chest pain. Although the patients do not succumb to an acute episode, unlysed thrombus in the pulmonary artery could eventually lead to chronic pulmonary hypertension; a syndrome of progressive right heart failure and corpulmonale (this condition develops when pulmonary embolism is either not diagnosed or is treated inadequately). Smaller pulmonary embolisms can result with occlusions of small peripheral pulmonary arteries. Bronchoconstriction can result from smaller pulmonary embolisms and collateral flow via bronchial vessels may not be preserved which could lead to pulmonary infarction. The clinical diagnosis of a pulmonary embolism is routinely confirmed by either a lung scan or pulmonary angiography. Typically, symptoms and signs develop three to seven days after the onset of an embolism. Treatment of the embolism is usually by anticoagulation for one to three weeks together with use of analgesics and supportive care.
Clinical suspicion is an important step toward diagnosis of a pulmonary embolism. Over-diagnosis or under-diagnosis can occur because signs and symptoms often are not maintained long enough to discriminate between patients with true pulmonary embolism and those without pulmonary embolism. The most common symptoms are shortness of breath, pleuritic chest pain, apprehension, and coughing. The most common signs are tachypnea (fast breathing) with a respiration rate (RR&gt;16/min), Rales, accentuated second heart sound, and tachycardia.
Perfusion lung scanning is an important diagnostic test in screening for pulmonary embolism. A normal lung scan essentially rules out most pulmonary embolisms and directs clinical attention to other diagnostic possibilities. Abnormal lung scans are categorized as being (1) low probability of pulmonary embolism, (2) moderate probability of pulmonary embolism, and (3) high probability of pulmonary embolism. As a general practice, patient's with a high probability of pulmonary embolism are treated with intravenous heparin (a blood thinner), patient's with a low probability of pulmonary embolism are not treated, and patient's with a moderate probability of a pulmonary embolism are either further evaluated with pulmonary angiography or are treated with intravenous heparin if angiography is not available and clinical suspicion is high. Pulmonary angiography has been considered the definitive test for the diagnosis of pulmonary embolism; however, the equipment needed is typically only available at large tertiary hospitals and university centers and is under-used even where it is available. The largest prospective study comparing abnormal lung scan and pulmonary angiography, performed by Hull et al. at Duke University, had the following results: 66% of the patient's with high probability of pulmonary embolism lung scans had a positive angiogram, 32% of patient's with moderate probability of pulmonary embolism lung scans had a positive angiogram, and 15% of the patient's with low probability of pulmonary embolism lung scans had a positive angiogram (note, as discussed above, these people would not ordinarily be treated). Moreover, 39% of the patient's with indeterminate lung scans had positive angiograms. Hence, the Hull et al. data underlines the importance of making pulmonary angiography more widely available.
Other modalities that are helpful in pulmonary embolism diagnosis are doppler echocardiogram computed tomography, digital substraction angiogram, magnetic resonance imaging, indium labeled platelet imaging, fiberoptic angioscopy. The presence of arterial blood gases, analysis of pleural fluid, electrocardiogram, blood tests, and chest X-rays can also indicate the presence pulmonary embolism. Tests used to diagnose deep venous thrombosis in the legs and pelvis include impedance plethysmography, B-mode ultrasonography and venography.
Patient's with certain risk factors are strongly predisposed to deep venous thrombosis and pulmonary embolism. Hypercoagulable states are the primary risk factors and they include antithrombin III deficiency, protein C and protein S deficiency, lupus anticoagulant, and deficiencies of minor blood factors. Secondary risk factors include abnormalities of coagulation and fibrinolysis such as malignancy, pregnancy, use of oral contraceptives, infusion of prothrombin concentrates, and nephrotic syndrome, abnormalities of platelets associated with myeloproliferative, diabetes mellitus, and heparin induced thrombocytopenia, and abnormalities of blood vessels and rheology. Conditions which promote venous stasis include immobilization, obesity, advanced age, and post operative state. Other conditions resulting in secondary hypercoagulable states include artificial surfaces such as grafts, vasculitis and chronic occlusive arterial disease, homocystinuria, hyperviscosity associated with polycythemia, leukemia, sickle cell disease, leukolutination, and increased serum viscosity.
Patient's with certain clinical conditions are predisposed to pulmonary embolism. For example, patient's who have had hip surgery, stroke or cerebral hemorrhage, major trauma, major abdominal or pelvic surgery, neurosurgery, neoplasm, sepsis, or cardiorespiratory failure all are at risk of developing pulmonary embolism. In addition, patient's that are immobilized, obese, over age 65, or have chronic medical conditions (cardiac, respiratory, or gastrointestinal) are predisposed to developing pulmonary embolism. Malignant cells, air, fat, bone marrow, amniotic fluid, tissue sites of injury, parasites and foreign materials are still other sources of pulmonary embolism.
As these risks and conditions have been identified, strong focus has been put on the prevention of deep venous thrombosis in high risk subgroups. Preventive treatment has resulted in a decreased incidence of pulmonary embolism in the last decade, but the decline has not been of a sufficient magnitude to attain acceptable levels. Conventional medical support in patients with pulmonary embolisms includes analgesia, oxygen, positive airway pressure, intubation for oxygenation or ventilation (which are unsatisfactory when unassisted), hyperventilation, positive end-expiratory pressure, and volume expansion. Blood thinners such as heparin have been used to treat pulmonary embolism for the past two decades. Heparin does not lyse the clot, but prevents clot enhancement and propagation and allows the patient's fibrinolytic system to stabilize and dissolve the clot over a period of time.
Unfortunately, based on most angiographic series, 30% to 60% pulmonary emboli are anatomically massive. As hemodynamic profile is more important, and underlying cardiopulmonary disease and humoral responses have significant influence, in autopsy series among all patient's dying from fatal pulmonary emboli, whether death occurs suddenly or more slowly, only half of the pulmonary embolisms meet the anatomical definition of massive.
In 1973 and 1974, urokinase and streptokinase, which are agents that cause clotting lysis, were investigated by the National Heart, Lung, and Blood Institute in the UPSET trial. Mortality from massive pulmonary embolisms was 33%; and whether heparin, urokinase, heparin or vena caval interruption, or heparin-streptokinase-embolectomy were used to treat massive pulmonary embolisms without shock, the mortality ranged from 5% to 7.7%. Also, apart from the transient immediate improvement in hemodynamics, the long-term survival between patients treated with thrombolysis and other aggressive measures or with traditional heparin therapy was the same. Moreover, patients treated with streptokinase and urokinase had more bleeding complications. It is estimated that only 10% of the patients with massive pulmonary embolisms survive long enough for angiographic analysis. However, the patients who do survive long enough to be diagnosed have benefitted from thrombolytic therapy, and in 1977 the Food and Drug Administration (FDA) approved the use of thrombolytic agents for pulmonary embolism.
More recently, tissue plasminogen activator (TPA), a selective thrombolytic agent which has been used nationwide for acute coronary thrombolysis, has been used to treat pulmonary embolisms. Dr. Goldhaber, at Harvard University, analyzed thirty six patients who were treated with TPA. It was noted that TPA treatment led to hemodynamic and angiographic improvement; however, only unilateral pulmonary angiograms were studied and only healthier patients were studied in that patients in shock (defined has having a systolic pressure less than 80 mm Hg) were not included in the investigation. In a recent report (1988) from a multicenter trial by Verstraete in Europe, TPA was given to 34 patients. Unfortunately, only four patients received thrombolysis within six hours of diagnosis, which is the most effective time for treatment. Nevertheless, the majority of patients were treated with TPA within 12-72 hours and a substantial number of them showed hemodynamic and angiographic improvement.
The chief surgical treatment for pulmonary embolism is embolectomy, i.e., surgical removal of the emboli. Even though this surgery was first performed in 1908, only after cardiopulmonary bypass was developed did it become standard therapy. Because of the critical state of the patients, embolectomy has a mortality rate of 25% to 50%. In a small group of patients, Dr. Greenfield and co-workers employed transvenous suction techniques for removal of emboli. In the transvenous suction experiments performed by Dr. Greenfield, embolic material was successfully removed from 13 of the fifteen patients (87%); however, four of the fifteen patients died.
Preventive surgical measures include ligation, plication or external clipping of the inferior vena cave, so that emboli can be prevented from propagating upstream. Inferior vena cava filters, which are permanent filters surgically placed in a patient predisposed to having recurrent encounters with pulmonary embolism as a preventive measure, have been employed for the last fifteen years. Examples of these types of filters include the Mobid-Uddin umbrella, the Kimray-Greenfield vena cava filter, and the Gunther vena caval filter. The following patient conditions may lead a physician to install an inferior vena caval filter for prophylaxis: a patient having a pulmonary embolism or extensive deep venous thrombosis and absolute contraindication for anticoagulation, a patient suffering from major bleeding on anticoagulation for embolism or venous thrombosis, a patient having a recurrent embolism leading to hemodynamic compromise, a patient with failure of adequate anticoagulation to prevent recurrent thromboembolic disease, a patient with chronic corpulmonale from multiple pulmonary emboli, a patient with a septic embolism, or a patient who has had an embolectomy. In a study of 1133 patients who have been provided with inferior vena cava filters 44% received them due to complications or failure of anticoagulation, 23% received them because of heparin was contraindicated, 13% received them because of caval/iliofemoral vein thrombosis, 8% received them as a prophylactic measure, and 8% received them due to severe pulmonary embolism during initial therapy.
Even though inferior vena caval filters have been in use for over a decade, their popularity is on the decline. These filters are left in the patient for life and lead to venous stasis and form a nidus for recurrent embolization. The Mobid-Uddin filter has been withdrawn because it had an operative mortality rate of 15% and recurrent embolization rate of 45%. The Kimray-Greenfield filter has had more favorable results with an operative mortality rate of 5%, venous problems of 38%, and recurrent embolization of 4%.
No products are currently available which can be used to temporarily prevent a pulmonary embolism in the clinical setting. For example, an obese women who has fallen down a flight of stairs, suffered injuries to her lower extremities, and has laid in bed for several days before reporting to the hospital in a bloated condition is very likely, as discussed above in conjunction with the risk factors and conditions which predispose a patient to a pulmonary embolism, to suffer a pulmonary embolism during routine surgery on her lower body. Other such patients, i.e, car accident victims, etc., are regularly encountered by the physician in the emergency room. What is needed is a device which the physician can use to temporarily protect the patient during the risk period for pulmonary embolism such as during and after surgery, but which can be easily removed when the patient is clear of the danger of a pulmonary embolism.